We intend to clarify the mechanism by which aliphatic amines cause myocardial damage by developing and extending our previous work on the cardiotoxicity of allylamine (AA). We will test our hypothesis that AA-induced acute myocardial necrosis is caused by vasospasm of medium-sized intramyocardial arteries which is mediated through toxic effects of AA or an AA metabolite on smooth muscle cells. Our approach includes ultrastructural, and morphometric characterization of the vessels, hemodynamic and blood flow measurements, and assessment of effects on AA-induced myocardial injury produced by compounds with smooth muscle action. We will examine the role of the myocardial enzyme monoamine oxidase (MAO) in this AA model of cardiotoxicity by characterizing "A and B" type MAO and benzylamine oxidase through a discriminating histochemical technique, through specific subcellular localization of these enzymes by ultracytochemistry, and through biochemical analysis of isolated cell subfractions. We will determine the in vivo fate of AA using 14C-AA an histoautoradiography and also determine if toxic metabolites of AA are formed. We will employ these techniques and investigative approach to explore several aliphatic amines which we suspect of having cardiotoxic properties. These include: (1) mono-, di-, and tri-ethylamine, compounds which in an older study were shown to induce pathologic cardiac lesions; (2) cyclohexylamine, a metabolite of the noncaloric sweeting agent cyclamate, which has been shown to have sympathomimetic action; and (3) isopropylamine, a metabolite of the drug propranolol.